Document Type
Honors Thesis
Abstract
Mitochondria have vital cellular functions, notably, the generation of energy dysfunctional mitochondria can activate the mitochondrial unfolded protein response (UPRmt), a conserved transcriptional response that regulates the expression of several mitoprotective genes. Research has shown that UPRmt activation promotes lifespan extension and increases resistance to infection. We recently discovered that loss of methionine synthase gene metr-1 activates the UPRmt. We performed a forward genetics screen to isolate modulators of the UPRmt caused by the metr-1 mutant. This was performed to determine how the loss of methionine synthase impacts the UPRmt and longevity. Interestingly, one mutant was isolated from this screen (named osa51), which enhanced the UPRmt in the metr-1 mutant background. The goal is to characterize this new mutant and attempt to identify the causative gene. Lifespan and developmental analyses yielded data showing the osa51 mutant strain had a significantly shorter lifespan and developed slower than the wild-type strain.
Publication Date
5-1-2021
Language
English
License
This work is licensed under a Creative Commons Attribution-NonCommercial-Share Alike 4.0 International License.
Recommended Citation
Zakaria, Heba, "IDENTIFICATION AND CHARACTERIZATION OF A MUTATION THAT ENHANCES THE MITOCHONDRIAL UPR RESULTING FROM LOSS OF METHIONINE SYNTHASE IN C. ELEGANS" (2021). 2021 Spring Honors Capstone Projects. 33.
https://mavmatrix.uta.edu/honors_spring2021/33